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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Dysregulated splicing factor SF3B1 unveils a dual therapeutic vulnerability to target pancreatic cancer cells and cancer stem cells with an anti-splicing drug

Fig. 3

Effect of SF3B1 modulation on PDAC cell lines. A Proliferation rates of HPDE E6E7, Capan-2, BxPC-3, and MIAPaCa-2 cell lines after SF3B1 silencing compared with scramble control-silenced cells (set at 100%; dotted line; n = 3–4). B Proliferation rates of same cell lines treated with or without (vehicle, set at 100%; dotted line) Pladienolide-B (n = 3–5). C Gemcitabine (Gm) and Pladienolide-B plus Gemcitabine (Pd + Gm) treated cells compared with vehicle-treated cells (set at 100%; dotted line; n = 3–5). D Migration rates of HPDE E6E7, Capan-2, BxPC-3 and MIAPaCa-2 cell lines treated with or without (vehicle; set at 100%) Pladienolide-B for 24 h. Representative images of wound closures (n = 4). E Quantification of sphere formation capacity of MIAPaCa-2 treated with Pladienolide-B or vehicle (control; set at 100%). Representative images of spheres (n = 4). F Colony formation capacity quantification of MIAPaCa-2 treated with Pladienolide-B or with vehicle (control; set as 100%). Representative images of colony formation (n = 3). G Apoptosis quantification using Caspase-3/7 assay in HPDE E6E7 and MIAPaCa-2 treated 24 h with Pladienolide-B or vehicle (control; set as 100%) (n = 4). Representative images show MIAPaCa-2 nuclear staining with DAPI. Data represents mean ± SEM. Asterisks indicate significant differences (*p < 0.05; **p < 0.01; ***p < 0.001)

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